Obstructive Sleep Apnea-Dependent and -Independent Adrenergic Activation in Obesity

Clinica Medica, Dipartimento di Medicina Clinica, Prevenzione e Biotecnologie Sanitarie, Università Milano-Bicocca, Ospedale San Gerardo, Monza, Milan, Italy.
Hypertension (Impact Factor: 6.48). 08/2005; 46(2):321-5. DOI: 10.1161/01.HYP.0000174243.39897.6c
Source: PubMed


No agreement exists as to the mechanisms responsible for the sympathetic hyperactivity characterizing human obesity, which has been ascribed recently to a chemoreflex stimulation brought about by obstructive sleep apnea rather than to an increase in body weight, per se. In 86 middle-age normotensive subjects classified according to body mass index, waist-to-hip ratio, and apnea/hypopnea index (overnight polysomnographic evaluation) as lean and obese subjects without or with obstructive sleep apnea, we assessed via microneurography muscle sympathetic nerve traffic. The 4 groups were matched for age, gender, and blood pressure values, the 2 obese groups with and without obstructive sleep apnea showing a similar increase in body mass index (32.4 versus 32.0 kg/m2, respectively) and waist-to-hip ratio (0.96 versus 0.95, respectively) compared with the 2 lean groups with or without obstructive sleep apnea (body mass index 24.3 versus 23.8 kg/m2 and waist-to-hip ratio 0.77 versus 0.76, respectively; P<0.01). Compared with the nonobstructive sleep apnea lean group, muscle sympathetic nerve activity showed a similar increase in the obstructive sleep apnea lean group and in the nonobstructive sleep apnea obese group (60.4+/-2.3 and 59.3+/-2.0 versus 40.9+/-1.8 bs/100 hb, respectively; P<0.01), a further increase being detected in obstructive sleep apnea subjects (73.1+/-2.5 bursts/100 heart beats; P<0.01). Our data demonstrate that the sympathetic activation of obesity occurs independently in obstructive sleep apnea. They also show that this condition exerts sympathostimulating effects independent of body weight, and that the obstructive sleep apnea-dependent and -independent sympathostimulation contribute to the overall adrenergic activation of the obese state.

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    • "Alvarez et al. did not see increased SNS activity despite higher levels of leptin in the subcutaneously obese individuals.[45] Another factor which is common in obesity and has been reported to contribute to the increased SNS activity is obstructive sleep apnea (OSA).[4046474849] However, this may again be related to the presence of visceral fat. "
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    • "Espino et al. (2011) showed that melatonin could reduce insulin secretion during sleep, preventing the development of obesity . Human obesity is also characterized by marked sympathetic activation (Grassi et al. 2005). Cardiac sympathetic activity was increased by weight gain during wakefulness and sleep (Adachi et al. 2011). "
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    • "Extracellular volume overload may contribute to SNS overactivity in CKD and ESRD by causing nocturnal rostral fluid shifts and peripharyngeal edema [78], resulting in obstructive sleep apnea (OSA), a highly prevalent condition in the ESRD population [79]. Multiple studies have shown that muscle sympathetic nerve activity (MSNA) is chronically elevated in patients with OSA [80–82], and more recently, a significant correlation was found between OSA and resistant hypertension among ESRD patients [83]. Adequate dialysis, volume control, and treatment of obstructive sleep apnea should be standard practice and may help ameliorate SNS overactivation in ESRD. "
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